正常食欲的肠-大脑轴机制是由金酸诱导的
Linghui Pan1, Ruihua Li1, Qiqi Li1
1Guangdong Provincial Key Laboratory of Animal Nutrition Control, National Engineering Research Center for Breeding Swine Industry and State Key Laboratory of Swine and Poultry Breeding Industry, College of Animal Science, South China Agricultural University, Guangzhou 510642, China.
Cell reports
|May 3, 2025
概括
肠道微生物产生氨酸 (KYNA),这增加了禁食期间的食欲. 基纳通过GPR35受体发出信号,激活控制食物摄入的大脑通路.
科学领域:
- 微生物学 微生物学
- 神经科学是一个神经科学.
- 代谢过程中的代谢.
背景情况:
- 食和肠道微生物群对于宿主生存至关重要.
- 肠道微生物代谢物可以影响宿主生理学.
- 食欲调节是一个复杂的过程,涉及神经和代谢信号.
研究的目的:
- 研究肠道微生物代谢物金酸 (KYNA) 在禁食期间调节食欲中的作用.
- 阐明神经通路和分子机制,通过这些神经通路和分子机制,KYNA会影响养行为.
主要方法:
- 在禁食期间测量肠道KYNA水平.
- 阴道神经操纵 (腹膜下阴道切除术).
- 化学基因操纵阴道 afferent 和弧形核 (ARCAgRP) 神经元.
- 在 afferent神经中,GPR35受体被淘汰.
- 电生理学记录和行为测试.
主要成果:
- 禁食显著增加了肠道KYNA水平.
- 通过肠道给予KYNA可增强短期的食物摄入量.
- 基纳的氧化作用通过抑制阴道 afferent 信号和激活 ARC AgRP 神经元来介导.
- 这些效应取决于神经和特定神经回路中的GPR35受体表达.
结论:
- 氨酸 (KYNA) 作为肠道微生物群向宿主传递信号的分子,在禁食期间调节食欲.
- 肠道微生物群-大脑轴涉及KYNA通过GPR35作用于状 afferent神经来调节养行为.
- 这项研究揭示了一种新的机制,将肠道微生物代谢物与主机食欲控制联系起来.
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